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Specialties > Anaesthetics > Flashcards

Anaesthetics Flashcards

1
Q

What do general anaesthetics do?

A

Produce insensibility in the whole body usually causing unconsciousness

Centrally acting drugs (analgesics/hypnotics)

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2
Q

What do regional anaesthetics do?

A

Produce insensitivity in an area or region of the body

E.g. blocking central/peripheral nerves

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3
Q

What do local anaesthetics do?

A

Produce insensibility in only the relevant part of the body

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4
Q

What is the triad of anaesthesia?

A

Hypnosis
Analgesia
Relaxation

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5
Q

Hypnosis

A

Sleepiness/unconsciousness

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6
Q

Analgesia

A

Lack of pain

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7
Q

Relaxation

A

Of skeletal muscle specifically

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8
Q

What agents cause hypnosis?

A

GA

Opiates can cause a little bit

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9
Q

What agents cause analgesia?

A

Opiates

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10
Q

What agents cause relaxation?

A

Muscle relaxants

GA a little too

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11
Q

Do you need to give analgesia even if the patient is unconscious?

A

Yes to prevent reflex autonomic responses to painful stimuli

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12
Q

What is involved in balanced anaesthesia?

A 
Different drugs do different jobs
Titrate doses separately 
Avoid OD (can use lesser doses when using diff drugs for diff things)
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13
Q

What are the problems with modern day anaesthetics?

A

Polypharmacy (DDIs/allergies)
Muscle relaxation - req. artificial ventilation and airway control
Separation of relaxation and hypnosis - awareness

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14
Q

What is awareness?

A

Paralysis of someone with muscle relaxants but they are still awake

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15
Q

How to GA work?

A

Interfere with neuronal ion channels
Open chloride channels –> hyperpolarise –> less likely to fire –> less action at synpases

(reversible)

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16
Q

How do inhalational GA work?

A

Dissolve in membranes

Confirmation of chloride channel changes so it opens

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17
Q

How do IV GA work?

A

Allosteric binding (binding to receptors at a place other than their active site)

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18
Q

How does Propofol work?

A

Binds to and agnosises GABA receptors

GABA receptors are chloride channels that hyperpolarise neurons and function as inhibitory CNS receptors

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19
Q

How is cerebral function lost with GA?

A

From top down - complex processes first, with relative sparing of primitive functions (reflexes/ANS)

Can still do reflexes on GA patient!

Loss of consciousness first, then hearing

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20
Q

Why are reflexes spared in GA?

A

They are primitive and have a small no. of synapses

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21
Q

What things must you do if you are giving GA?

A

Airway req.
Temp control
Avoid pressure sores
Keep them comfortable

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22
Q

How quickly do IV anaesthetics work?

A

Rapidly - v. fat soluble - cross BBB
1 arm brain time (brain so well perfused)

ALSO clears quickly! - mainly due to drug leaving circulatory compartment and into vessel rich tissues, then skeletal muscle so conc. in blood falsl quickly)

After while goes into fat (fat poorly perfused so takes while to accumulate there)

Goes back into blood, metabolised by liver

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23
Q

Giving IV anaesthetics requires…

A

Constant infusion

Target controlled infusion pump allows for v accurate infusion to achieve specific blood/brain concs.

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24
Q

What are the inhaled anaesthetics?

A

Halogenated hydrocarbons

Breathed in and out of lungs

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25
Q

How do inhaled anaesthetics get to the brain?

A

Conc. gradients - lungs > blood > brain

Cross alveolar BM easily

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26
Q

MAC

A

Minimal alveolar concentration (conc of drug in alveoli which is req. to produce anaesthesia)

Measure of potency

Low no = high potency

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27
Q

Inhalational anaesthetics

A

Induction slow

Are used to extend/continue anaesthesia

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28
Q

How are the effects of inhalational anaesthetics reversed?

A

Washout - reversal in concentration gradient –> fall in alveolar concentration, followed by blood, brain and then consciousness returns

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29
Q

Most people have ____ induction and _____ maintenanc

A

IV
Inhalation

Rapid onset of IV induction, flexibility and more control with inhalation

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30
Q

What are the CVS effects of GA?

A

Central - depression of CNS, CV centres & nuclei –> reduced SNS ouflow, negative inotrophic/chronotrophic effect on heart (dec. HR), reduced vasomotor tone –> vasodilation

Direct - anaesthesia on vascular smooth muscle & myocardium - negatively inotropic, vasodilation –> decreased peripheral resistance, venodilation –> reduced venous return, decreased CO

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31
Q

MAP = ?

A

CO x SVR

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32
Q

What are the respiratory effects of GA?

A

Resp depression
Reduce hypoxic and hypercarbic drive via depression of brainstem resp centres –> decreased TV and increased rate
Paralysis of cilia
Decreased FRC - lower lung volumes –> VQ mismatch

May req. O2 post op

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33
Q

When are muscle relaxants indicated?

A 
When ventilation and intubation req. 
Immobility essential (e.g. microscopic surgery, neurosurgery, body cavity surgery
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34
Q

What are the problems with muscle relaxants?

A

Awareness
Incomplete reversal - airway obstruction/ventilatory insufficiency in immediate post-op period
Apnoea - dependence on airway and ventilatory support

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35
Q

Why do you give intraoperative analgesia?

A

Prevention of arousal
Opiates contribute to hypnotic effect
Suppression of reflex responses to painful stimuli - tachycardia, HTN –> more bleeding in an op

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36
Q

In regional/local anaesthesia - derangement of CVS physiology is proportional to what?

A

Size of anaesthetised area

There is relative sparing of aresp function

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37
Q

How do regional anaesthetics usually provide muscle relaxation?

A

Blocking motor nerves so spinal or epidural anaesthesia may not req. muscle relaxants

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38
Q

What is the limiting factor in the use of local anaesthetics?

A

Toxicity (high plasma levels, e.g. absorption > rate of metabolism)

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39
Q

What does toxicity of LA depend on?

A

Dose used
Rate of absorption (site dependent)
Patient wt
Drugs (bupivacaine > lignocaine > prilocaine)

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40
Q

What are the ssx of LA toxicity?

A

Circumoral/inguinal numbness/tingling, light headedness, tinnitus, visual disturbances, muscular twitching, drowsiness, CV depression, convulsions, coma, cardiorespiratory arrest

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41
Q

LA: differential blockage

A

Diff penetration into diff nerve types

Myelinated, thick fibres relatively spared –> motor fibres relatively spared, pain fibres blocked easily –> anaesthesia without paralysis

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42
Q

What are the CVS effects of RA?

A

All due to symphathectomy due to LA blockage of mixed spinal nerves –> veno and vasodilation

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43
Q

Give e.g.s of RA

A

Field blocks, e.g. hernia repair
Plexus block
Limb blocks, e.g. femoral/sciatic
Central neural block, e.g. epidural, spinal

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44
Q

What is the physiology of a neuroaxial block?

A

Inspiratory function spared (insp muscles served by higher roots)
Expiratory function impaired (cough dependent on abdo muscle function)
Decreased FRC
Increased VQ mismatch

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45
Q

Conduct of GA

A 
Pre-op assessment 
Preparation
Induction 
Maintenance
Emergence
Recovery 
Post-op care and pain manage
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46
Q

What is involved in preparation?

A 
Planning
Right patient, side, operation 
Pre-meds (analgesia e.g.) 
Right equipment, personnel
Drugs drawn up 
IV access 
Monitoring
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47
Q

What is involved in induction?

A

Gas/IV
Monitor consciousness
Airway maintenance

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48
Q

What drugs are used for IV induction?

A

Propofol (most used), thiopentone (barbiturate), others

May also give benzodiazepine, muscle relaxants, analgesia

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49
Q

What drugs are used in gas induction?

A

Halothane

More common in kids/IVDA where venous access difficult

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50
Q

What are the planes of anaesthesia?

A

Analgesia/sedation - light headed, giggly, eyes may close
Excitation (disinhibited)
Anaesthesia (deep –> light)
Overdose (too deep, serious cardio and resp depression)

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51
Q

How do you monitor conscious level?

A 
Loss of verbal contact
Movement
Resp pattern 
Processed EEG
Stage/plane
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52
Q

What is involved in airway management in anaesthesia?

A

Tongue normally held by tone –> anaesthesia –> falls back and obstructs airway

HEAD TILT/CHIN LIFT/JAW THRUST

Simple apparatus - face mask, oropharyngeal (Guedel) airway, nasopharyngeal airway

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53
Q

Anaesthetic face mask

A

Gas tight seal

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54
Q

Oropharyngeal airway

A

Rigid plastic
ONLY when unconscious

In light plane insertion may –> vomiting, laryngospasms

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55
Q

Laryngeal mask airway

A

Cuffed tube with mask sitting over glotting

Maintains but does not protect airway

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56
Q

What is the standard airway device kept on the red trolley?

A

I-gel

2nd gen LMA

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57
Q

What are airway complications in GA use?

A

Obstruction - ineffective triple airway manoeuvre most common cause, airway device/kinking/laryngospasm

Aspiration - loss of protective airway reflexes, foreign material in lower airway (blood, gastric contents, surgical debris)

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58
Q

Distinguish between airway maintenance and airway protection

A

Maintenance - open and patent

Protection - cuff tube in trachea protects airway from contamination

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59
Q

What is the only protected airway maintenance?

A

Endotracheal intubation

Laryngeal reflexes must be abolished

Laryngoscope, muscle relaxant, sniffing the morning air position

Or LA, fibre optic scope

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60
Q

Why intubate?

A

Protect from gastric contents in non-fasted patient
Need for muscle relaxant & artificial ventilation
Shared airway with risk of contamination, e.g. tonsillectomy
Need for tight control of BG (e.g. CO2 levels in neurosurgery)
Restricted access to airway, e.g. MaxFax

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61
Q

What are risks to an unconscious patient?

A 
Airway
Temperature
Loss of other protective reflexes
VTE risk 
Consent and identification 
Pressure areas
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62
Q

What are the different positions patients can be in?

A 
Supine
Lithotomy
Prone
Lying on side
Sitting
63
Q

What is involving in continuing anaesthesia?

A 
Care of unconscious person
Analgesia, muscle relaxants
Fluid management
Monitoring and physiological support
Documentation 
Maintenance (IV/inhalation/both)
Self/artificial ventilation 
Analgesia 
Gas supply from anaesthetic machine
64
Q

What is involving in monitoring when someone is under anaesthesia?

A

Basic minimum - SpO2, CG, NIBP, FiO2, ETCO2
Respiratory parameters
Agent monitoring
Temp, UO, NMJ with nerve stimulator
Invasive venous/arterial monitoring to measure pressure
Processed EEG
Ventilator disconnect alarm

65
Q

What are the anaesthetic complications?

A 
Airway 
Breathing
Circulation 
Related to technique/position
Awareness
66
Q

How common is awareness?

A

1 in 42, 000

67
Q

What are risk factors for awareness?

A

Paralysed and ventilated, prev. episode of awareness, chronic CNS depressant use, cardiac surgery, major trauma, GA C-section

68
Q

What happens in emergence?

A 
Muscle relaxant reversed
Anaesthetics ware of 
Resumption of spontaneous respiration 
Return of airway reflexes/control
Extubation  (if removed prematurely risk of laryngospasm)

Can be v. quick of slow (depends on dose, inter-individual variation)

Worry if prolonged emergence

69
Q

What is involved in recovery?

A

May have not regained consciousness/airway control
ABC problems
Pain control
Post op NV

70
Q

What are your Na requirements?

A

1-2mmol/kg/day

71
Q

What are your K requirements?

A

0.5-1mmol/kg/day

72
Q

What are your fluid req.?

A

25-30ml/kg/day

73
Q

What are your glucose req.?

A

50-100g/kg/day

74
Q

What are the levels of critical care?

A 
Levels of care:
0 - primary care
1 - ward care
2 - HDU
3 - ITU

HDU = single organ support
ITU = multi-organ support
Both of these are critical care

75
Q

Under what circumstance with single organ failure would you come to ITU?

A

If you req. invasive ventilation

76
Q

What is your plan with a compromised airway?

A

Head tilt, chin lift, jaw thrust

Oropharyngeal airway

Then get anaesthetics to intubate

77
Q

Distinguish between type 1 and type 2 respiratory failure

A

type 1 - one problem, low O2 in the blood

Type 2 - 2 problems - low O2 high CO2

Because CO2 passes out the blood easily type 1 most common

78
Q

What is your approach to tachypnoea/respiratory distress?

A

Blood gas to see if hypercapnic

If issue with oxygenation - high flow nasal cannula, CPAP, intubation and invasive ventilation, ECMO

If problem also involves CO2 removal then invasive ventilation tends to be req.

79
Q

CO = ?

A

HR x SV

80
Q

SV = ?

A

Preload/contractility/afterload

81
Q

What do vasopressors do?

A

Increase afterload

82
Q

What do inotropes do?

A

Drive contractility

83
Q

What do chronotropes do?

A

Speed up HR

84
Q

What do beta blockers do?

A

Slow HR

85
Q

How much fluids should you give in sepsis?

A

30ml/kg before switching to vasopressors

86
Q

What kind of drugs are vasopressors?

A

Alpha-1-agnosts
They constrict BVs

Mostly veins

87
Q

What kind of drugs are inotropes?

A

Beta-1-agonists –> improved contractility

88
Q

How can you measure the result of giving vasopressors/intropes etc. to improve circulation?

A

Better BP
UO - kidneys better perfused
Conscious level - brain perfused
Lactate reduced - less hypoperfusion

89
Q

What level of lactate is abnormal?

A

> 2

90
Q

What is involved in disability of ABCD?

A

Look at all the other organs, e.g. dialysis, TPN,

91
Q

GCS below what = intubation?

A

8

92
Q

GENERAL ANAESTHESIA

A

Drug induced reversible coma
CNS, cardiac and respiratory depression
DDIs

93
Q

REGIONAL ANAESTHESIA

A

Profound sympathectomy - obliterating BP and normal mechanisms to control BP
Neurological sequalae

94
Q

What is involved in pre-op care?

A 
Assess
High risk mortality/morbidity?
Minimise risk 
Inform and support patient decisions
Consent
95
Q

Why is pre-op care important?

A

Reduces anxiety, delays, cancellations, complications, mortality, length of stay

Identifies comorbs, limitations, red flags

96
Q

When is pre-op care done?

A

Elective: GP, pre-assessment clinic

Urgent less time

Emergency less time but must identify risks still

97
Q

What is done in pre-op assessment?

A

Hx - co-morbs, systemic enq for unknown comorbs, clinical Ex, ability to withstand stress (ETT, reasons for limitation, CR dx), DA, prev surgery/anaesthesia, potential issues - airway, spine, reflux, obesity, malignant hyperpyrexia, cholinesterase deficiency
Ix

98
Q

What is involved in Ix in pre-op assessment?

A

Detect unknown conditions, diagnose suspected conditions, severity of known disease, getting a baseline, assessing risk etc.

99
Q

What cardio Ix might you do in pre-op care?

A

ECG, ETT, echo, myocardial perfusion scans, stress echo, cardiac catheterisation, CTCA

100
Q

What resp Ix might you do in pre-op assessment?

A

Sats, ABG, CXR, peak flow measurements, FVC, FEV, gas transfer, CT chest

101
Q

What is ASA grading?

A 
ASA 1 - otherwise healthy patient 
ASA 2 - mild to moderate systemic disturbance
ASA 3 - severe systemic disturbance
ASA 4 - life-threatening dx
ASA 5 - moribund patient 
ASA - organ retrieval
102
Q

What is cardiac risk index?

A

Estimates likelihood of perioperative cardiac events

1 point for each of:
High risk surgery 
Ischaemic heart dx
Congestive heart failure
CV dx
Diabetes
Renal failure

0/1 point = 0.4-0.9&
2 points = 6 points
3+ = 11%

103
Q

What are the ETT METs?

A

Can you do the following without getting breathless:

walk around house - 2 METs
do light housework - 3 METs
walk 100-200m on flat - 4 METs
Climb a flight of stairs/walk uphill - 5 METs
Walk on flat at brisk pace - 6 METs
Play golf, mountain walk, dance/other exercise - 7 METs
Run a short distance - 8 METs
Do strenuous exercise/heavy physical work - 9 METs

5 or more - likely to have better outcomes than if less than 5

104
Q

What does cardiopulmonary exercise testing measure?

A

Expired/inspired O2 (strength and capacity of lungs), ECG, BP before, during and after exercise

Can predict outcomes of durgery

105
Q

What things do we want to optimise pre-operatively?

A

HTN, IHD, HF, asthma, COPD, DM, epilepsy

106
Q

What is poor diabetic control assoc with post-operatively?

A

Inc. risk of infections, cardiac and resp complications

107
Q

What lifestyle factors do you want to address in your pre-op assessment?

A

Smoking - less post-op resp complications if they stop
Alcohol - reduce and reduce risk of infection and septic shock
Obesity
Exercise - better outcomes

108
Q

High risk emergency patient pre-op care

A

Informed consent
Anaesthetic plan
Invasive monitoring more likely to be req.

109
Q

Pre-op medication

A

Continue as normal for most (esp inhalers, anti-anginals/epileptics)

Exceptions: oral hypoglycaemics, anticoagulants

110
Q

Define pain

A

Unpleasant sensory and emotional experience assoc with actual/potential tissue damaged

111
Q

How common is persistent pain?

A

1 in 4

Assoc. w v. poor QoL

112
Q

What is the most common cause of pain?

A

Lower back pain

113
Q

What are the benefits of treating pain for the patient?

A

Physical - improved sleep, better appetite, less medical complications (e.g. heart attack)
Psychological - less suffering, less depression/anxiety

114
Q

What are the benefits of treating pain for the family of the patient?

A

Improved functioning as family member

Able to keep working

115
Q

What are the benefits of treating pain for society?

A

Lower health costs

Able to contribute to community

116
Q

How is pain classified?

A

Duration - acute, chronic (>3m, after normal healing), acute on chronic

Cause - cancer/non-caner

Mechanism - nociceptive/neuropathic/mix

117
Q

What is nociceptive pain?

A

Pain due to damage to nociceptive afferents in tissue/skin
Obvious tissue damage
Aka physiological/inflammatory pain serves a protective function
Rx with WHO pain ladder

118
Q

What is neuropathic pain?

A

May not see obvious tissue damage
No protective function
Abnormality of nervous system (e.g. slipped disc)

119
Q

What is the character of nociceptive pain?

A 
Sharp +/- dull
Well localised (ab pain may be less localised if visceral)
120
Q

What is the character of neuropathic pain?

A

Burning, shooting +/- numbness, pins, needles

Not well localised

121
Q

Physiology of pain

A

PERIPHERY - tissue injury, release of chemicals (prostaglandins, substance P –> pain) - accentuate pain pathway (amplifying the signal), inflammatory pathway worsens sensation of pain by release of chemical markers
Stimulation of pain receptors (nociceptors)
Signals travel in Adelta or C nerves to spinal cord

SPINAL CORD - first relay - Adelta/C nerve synapses with second nerve which travels up to spinal cord via spinothalamic tracts

BRAIN - thalamus is second delay station - connects to thalamus, limbic system, brainstem (inc. BP, tachycardia)
Pain perception in cortex

MODULATION - descending pathway from brain to dorsal horn, usually descreases pain signal
Genetic difference in modulation - some better at descending inhibition (less sore)
Done through NA/5HT reuptake

122
Q

What is the gate theory of pain?

A

Noxious stimuli can be reduced by distractive stimuli (rubbing, massaging etc.) by Ab/a neurones creating a negative inhibition loop to switch off pain fibres

123
Q

What fibres carry noxious stimuli?

A

Adelta

C

124
Q

What fibres carry normal sensation?

A

Aalpha

Abeta

125
Q

What is neuropathic pain due to?

A

Abnormal processing of a pain signal due to NS damage/dysfunction
e.g. diabetic neuropathy, nerve trauma, fibromyalgia, chronic tension headache, common after thoracic surgery/mastectomy as intercostal nerves damaged

126
Q

What are the pathological mechanisms behind neuropathic pain?

A

Increased receptor numbers
Abnormal sensatisation of nerves (peripheral/central)

Things that do not normally cause pain (e.g. cold air) will
Damage to thalamic pathways after stroke –> chronic pain
Chemical changes in dorsal horn
Loss of inhibitory modulation, e.g. NA/5HT

127
Q

What are the classification of drugs for pain?

A

Simple anaglesics (paracetamol/NSAIDs)
Opioids (mild - codeine, dihydrocodeine, strong - morphine, fentanyl)
Others

128
Q

What are the adverse effects of NSAIDs?

A

Renal function, DDIs

129
Q

What are the other analgesics?

A

Tramadol
Antidepressants (amitryptilline, duloxetine for neuropathic pain)
Anticonvulsants (gabapentin)
Ketamine (NMDA receptor antagonist - works centrally in spinal cord)
LAs
Topical agents, e.g. capsaicin

130
Q

What are your Rx for pain working in the periphery?

A

RICE
NSAIDs
Local anaesthetics

131
Q

How do LAs work?

A

Switch of adelta/C fibres

132
Q

What are your Rx for pain working at the spinal cord?

A

Acupuncture, TENS, massage
LA
Opioids
Ketamine

133
Q

What are your Rx or pain working in the brain?

A

Psychological/CBT
Pain management programmes
Paracetamol, opioids, amitryptilline, clonidine

134
Q

Paracetamol - adv and disadv

A

Adv - cheap, safe, oral/rectal/IV administration
Good for mild pain or in combo with other drugs for more severe pain

Disadv - liver damage in OD

135
Q

NSAIDs - advs and disadvs

A

Adv - cheap, generally safe, nociceptive pain (best given with paracetamol - synergism)
Disadv - GI/renal SEs, plus sensitive asthmatics

136
Q

Give e.g.s of NSAIDs

A

Aspirin, ibuprofen, diclofenac

137
Q

Codeine - advs and disadv

A

Adv - cheap, safe, mild-mod nociceptive pain (best given with paracetamol)

Disadv - constipation, nausea, not good for chronic pain

138
Q

Tramadol - adv and disadv

A

Adv - less resp depression, can be used with opoids and single analgesics

Disadv - NV

139
Q

How does tramadol work?

A

Weak opioid effect plus inhibitor of serotonin/NA reuptake (modulation)

140
Q

Morphine - adv & disadv

A

Adv - cheap, safe, antedote if take too much, IM, IV, PO, SC
Good for mod-severe nociceptive pain, chronic cancer pain

Disadv - constipation, resp depression in high dose, oral dose 2-3x IV/IM/SC (lot taken away by first pass met)

141
Q

How does amitryptilline decrease pain?

A

Increases descending inhibitory signals

142
Q

Amitryptiline adv and disadv

A

Adv - cheap, safe, good for neuropathic pain
Also Rx depression, poor sleep

Disadv - anticholingeric SEs

143
Q

How do anticonvulsants reduce pain?

A

Reduce abnormal firing of nerves

Good for neuropathic pain

144
Q

What are the ways you can administer pain relief?

A 
Oral 
Rectal 
Sublingual 
Subcutaneous
Transdermal 
IM
IV
145
Q

What are delivery routes for local anaesthetics?

A 
Epidural 
Intrathecal 
Wound catheters
Nerve plexus catheters
Local infiltration of wounds
146
Q

What are the ways you can assess pain?

A

Verbal rating score (no pain, mild, mod, severe, excruitiating - 1 to 5)
Numerical rating score (0-10)
Visual analogue - 10cm line mark where pain is
Smiling faces in paeds (happy smiling child –> screaming)
Abbey pain scale (confused patients) - pain behaviour scoring, bad behaviour in dementia is largely down to them being sore

147
Q

What are non-drug Rx for pain?

A

RICE, surgery, acupuncture, massage, physio, changing their posture
Psychological - explanation, reassurance, counselling

148
Q

For what kind of pain do you use the WHO pain ladder?

A

Nociceptive acute pain

149
Q

How do you Rx neuropathic pain?

A

Alternative analgesics/psychological/non-drug Rx

150
Q

What is the WHO pain ladder?

A

Mild-mod pain - non-opioids (NSAIDs, paracetamol)

Mod-severe - mild opioids (codeine) +/- non-opioids

Severe - strong opioids (morphine) +/- non-opoids

151
Q

As pain resolves what do you with their pain relief?

A

Move down the ladder - passing middle rung first

Stop NSAIDs before paracetamol

152
Q

What is the RAT approach to pain management?

A

Recognise - are they in pain?
Assess - severity, type, other factors (depression, anxiety, substance misuse, social factors)
Treat

Reassess after

153
Q

What drugs should you use to Rx neuropathic pain?

A

Amitryptilline
Gabapentin
Duloxetine

Specialties (1 decks)

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